Secondary hyperparathyroidism (SHPT) is a well known complication to chronic renal failure. With impaired renal function the phosphate excretion from the kidney is reduced. Together with low levels of 25- and 1,25-vitamin D3 and hypocalcemia this uremic mineral milieu drives the release of parathyroid hormone (PTH) and the development of SHPT. PTH has many functions but acts mainly to release calcium from the skeleton, to enhance calcium uptake from the intestines (by actions on vitamin D) and to lower serum phosphate by inducing phosphaturia. SHPT has been shown to cause vascular morbidity and fractures in the chronic kidney disease (CKD) patient. After successful renal transplantation (RT) the mineral disturbances are mostly recovered and stabilized at one year post RT, but in recent years it has been shown that SHPT persists in the major part of RT-recipients even after long term follow up. This has been associated with high risk of fractures and vascular related morbidity in the post transplant period. It has also been shown that low levels of iPTH in the post-transplant period might be associated with a high risk of fractures. Because of insufficient data on PTH levels and associated morbidity there is no specific recommendations of target PTH levels in the RT-patient. This indicates that there is need for further observational studies to describe the SHPT-associated morbidity in a post transplant cohort based on stabilized levels of post transplant iPTH.